Leukotrienes as mediators in ischemia-reperfusion injury in a microcirculation model in the hamster.

Lehr, Hans‐Anton; Guhlmann, Albrecht; Nölte, D.; Keppler, Dietrich; Meßmer, K.

doi:10.1172/jci115233

Cited by 209 publications

(129 citation statements)

References 47 publications

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“…1 B ). Thus, PAF-like lipids, rather than authentic PAF (14,35), are generated in vivo in response to cigarette smoke, consistent with the recent demonstration of in vivo plasma lipid oxidation in smokers (22,24).…”

Section: Resultssupporting

confidence: 84%

“…Analysis of leukocyte interactions in the microcirculation (34) before smoke exposure and at the stated times after exposure was performed in four to six arterioles and venules (20-60 m diameter) per observation window. Leukocytes were visualized after intravascular injection of acridine orange (35) and cells remaining stationary at the vascular wall for 30 s were classified as adherent. Vessel diameters and red cell velocities were analyzed offline from video recordings as described (34).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Vitamin C blocks inflammatory platelet-activating factor mimetics created by cigarette smoking.

Lehr¹,

Weyrich²,

Saetzler³

et al. 1997

J. Clin. Invest.

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156

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Cigarette smoking within minutes induces leukocyte adhesion to the vascular wall and formation of intravascular leukocyte-platelet aggregates. We find this is inhibited by platelet-activating factor (PAF) receptor antagonists, and correlates with the accumulation of PAF-like mediators in the blood of cigarette smoke-exposed hamsters. These mediators were PAF-like lipids, formed by nonenzymatic oxidative modification of existing phospholipids, that were distinct from biosynthetic PAF. These PAF-like lipids induced

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Section: Resultssupporting

confidence: 84%

Section: Methodsmentioning

confidence: 99%

Vitamin C blocks inflammatory platelet-activating factor mimetics created by cigarette smoking.

Lehr¹,

Weyrich²,

Saetzler³

et al. 1997

J. Clin. Invest.

Self Cite

156

View full text Add to dashboard Cite

show abstract

“…In some instances a net increase in bacterial titer was preceded by lag times as long as [20][21][22][23][24][25][26][27][28][29][30] hours after the intracerebral inoculation of an inoculum of 10 3-104 cfu. Once bacterial growth commences, the time of onset ofCSF leukocytosis is a remarkably sensitive indicator of the bacterial concentration.…”

Section: How Microorganisms Challenge the Host In Bacterial Meningitismentioning

confidence: 99%

“…Attracted activated leukocytes may release cytotoxic products, such as reactive oxygen species, reactive nitrogen intermediates, and proteolytic enzymes, that may augment tissue damage, with subsequent edema formation. This leukocyteinduced tissue damage plays a role in a variety of disease processes, such as ischemia-reperfusion [30], atherogenesis [31], and bacterial meningitis [32,33].…”

Section: Leukocyte-endothelial Cell Interactionsmentioning

confidence: 99%

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Pfister

Fontana²,

Täuber³

et al. 1994

Clinical Infectious Diseases

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Morbidity and mortality associated with bacterial meningitis remain high, although antibiotic therapy has improved during recent decades. The major intracranial complications of bacterial meningitis are cerebrovascular arterial and venous involvement, brain edema, and hydrocephalus with a subsequent increase of intracranial pressure. Experiments in animal models and cell culture systems have focused on the pathogenesis and pathophysiology of bacterial meningitis in an attempt to identify the bacterial and/or host factors responsible for brain injury during the course of infection. An international workshop entitled "Bacterial Meningitis: Mechanisms of Brain Injury" was organized by the Department of Neurology at the University of Munich and was held in Eibsee, Germany, in June 1993. This conference provided a forum for the exchange of current information on bacterial meningitis, including data on the clinical spectrum of complications, the associated morphological alterations, the role of soluble inflammatory mediators (in particular cytokines) and of leukocyte-endothelial cell interactions in tissue injury, and the molecular mechanisms of neuronal injury, with potential mediators such as reactive oxygen species, reactive nitrogen species, and excitatory amino acids. It is hoped that a better understanding of the pathophysiological events that take place during bacterial meningitis will lead to the development of new therapeutic regimens.Although the recent licensure of Haeniophilus influenzae type b (Hib) polysaccharide conjugate protein vaccines has had a marked impact on the incidence of invasive Hib disease in the United States and Western Europe. bacterial meningitis overall remains a significant problem worldwide. In addition, despite the introduction of new antimicrobial agents and improved diagnostic techniques, the mortality and morbidity associated with bacterial meningitis remain unacceptably high. This discrepancy between a rapid bacteriologic response at the site of infection (i.e .. eradication of viable bacteria from the CSF due to treatment with potent bactericidal agents) and the persistence of the associated neurological sequelae and mortality has prompted intense investigation over the past two decades into the pathophysiology of this disease. Indeed. recent clinical studies have employed adjunctive agents (e.g .. dexamethasone) in an attempt to reduce mortality and alleviate neurological sequelae [1][2][3][4]. These studies and the resulting recommendations regarding the use of adjunctive dexamethasone have recently been reviewed [5.6].In line with the current emphasis on the pathogenesis and pathophysiology of bacterial meningitis. two workshops were held in California in the 1980s [7]. Recognizing that many advances have been made in this field in the several years since those meetings. the Department of Neurology at the University of Munich organized a similar workshop, which was held in Eibsce. Germanv. on 25 and 26 June 1993. As IS evident from its title-"Bacterial Meningitis: Mechanisms...

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“…Já a utilização de inibidores da lipooxigenase ou bloqueadores da ação de leucotrienos preveniu a lesão pulmonar. Lehr et al (79) sugeriram que a interação entre os neutró-filos e o endotélio na lesão de reperfusão é mediada por leucotrienos. Em modelo com "hamster", eles evidenciaram o acúmulo de leucotrienos na microcirculação após isquemia e reperfusão.…”

Section: Tabela 1 Situações Clínicas Associadas à Lesão De Isquemia-runclassified

Lesão pulmonar de reperfusão

Pinheiro

Holanda

Araujo³

et al. 1999

J. Pneumologia

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A lesão de isquemia-reperfusão constitui-se em um evento fisiopatológico comum a diversas doenças da prática clínica diária. O pulmão pode ser alvo da lesão de isquemia-reperfusão diretamente, como no edema pulmonar após transplante ou na resolução de tromboembolismo; ou ainda ser atingido à distância, como nos casos de choque ou por lesão de reperfusão em intestino ou em membros inferiores, como ocorre no pinçamento da aorta, utilizado nas cirurgias de aneurisma. Dentre os mediadores envolvidos na lesão de isquemia-reperfusão, foram identificados espécies reativas tóxicas de oxigênio (ERTO), mediadores lipídicos, como a tromboxana, moléculas de adesão em neutrófilos e endotélio, fator de necrose tumoral, dentre outros. As medidas terapêuticas para a lesão de reperfusão ainda são utilizadas no plano experimental e em poucos estudos clínicos. São utilizados: antioxidantes, bloqueadores de mediadores lipídicos, inibidores da interação entre leucócito e endotélio ou substâncias que favoreçam o fluxo sanguíneo pós-isquêmico. Pneumol 1999;25(2):124-136) Perfusion lung injury The ischemia-reperfusion injury is a common pathophysiologic phenomenon in many diseases seen in daily clinical practice. The lung can be affected both directly, as in pulmonary edema after lung transplant or after resolution of pulmonary thromboembolism, and indirectly, as in shock states or after reperfusion injury in distant organs

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Leukotrienes as mediators in ischemia-reperfusion injury in a microcirculation model in the hamster.

Cited by 209 publications

References 47 publications

Vitamin C blocks inflammatory platelet-activating factor mimetics created by cigarette smoking.

Vitamin C blocks inflammatory platelet-activating factor mimetics created by cigarette smoking.

Mechanisms of Brain Injury in Bacterial Meningitis: Workshop Summary

Lesão pulmonar de reperfusão

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